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Related Concept Videos

Telomeres and Telomerase02:41

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Telomeres and Telomerase02:41

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In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded...
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Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells NPCs
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Valproic Acid Induces Telomerase Reverse Transcriptase Expression during Cortical Development.

Ki Chan Kim1, Chang Soon Choi1, Edson Luck T Gonzales1

  • 1School of Medicine and Center for Neuroscience Research, SMART Institute of Advanced Biomedical Sciences, KU Open Innovation Center, Konkuk University, Seoul 05029, Korea.

Experimental Neurobiology
|November 3, 2017
PubMed
Summary

Valproic acid exposure increases telomerase reverse transcriptase (TERT) in developing rat brains, impacting neuronal development and autism spectrum disorder (ASD) phenotypes. This suggests TERT is a key player in VPA-induced autism models.

Keywords:
autismexcitatory/inhibitory imbalanceglutamatergic neuronal differentiationtelomerase reverse transcriptasevalproic acid

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Genetics

Background:

  • Autism spectrum disorder (ASD) presents significant challenges due to its complexity and lack of effective treatments.
  • The valproic acid (VPA)-induced animal model is crucial for studying environmental risk factors in ASD.
  • Previous research linked VPA exposure to increased Pax6 expression and subsequent glutamatergic marker changes.

Purpose of the Study:

  • To investigate the role of telomerase reverse transcriptase (TERT) in VPA-induced alterations relevant to ASD.
  • To elucidate the molecular mechanisms underlying TERT upregulation by VPA.
  • To determine TERT's direct involvement in VPA-induced changes in neuronal markers.

Main Methods:

  • Utilized Western blot, RT-PCR, and immunostaining to assess TERT expression in VPA-exposed rat brains and neural progenitor cells (NPCs).
  • Employed chromatin immunoprecipitation to analyze histone acetylation and HDAC1 binding to Pax6 and Tert genes.
  • Used Tert siRNA transfection in cultured NPCs to confirm TERT's functional role.

Main Results:

  • VPA exposure significantly increased TERT expression in embryonic rat brains and NPCs.
  • VPA's histone deacetylase (HDAC) inhibitor property was identified as the cause of TERT upregulation.
  • VPA increased histone acetylation and reduced HDAC1 binding to Pax6 and Tert genes.
  • Overexpression of TERT by VPA led to increased expression of neuronal markers (Ngn2, NeuroD1) and synaptic proteins (PSD-95, α-CaMKII, vGluT1, synaptophysin).
  • Silencing TERT with siRNA reversed VPA-induced changes in NPCs.

Conclusions:

  • TERT is implicated in the VPA-induced autistic phenotypes observed in animal models.
  • TERT acts as a critical modulator of neuronal development and synaptic transmission disrupted by VPA.
  • Findings highlight TERT as a potential therapeutic target for ASD-related neurodevelopmental abnormalities.